In patients with LSS, their genetic profile significantly correlated with the upregulation of Laminin subunit alpha-4 (LAMA4) and Sushi-repeat containing protein x-linked-2 (SRPX2) gene that provoked ECM degradation and the downregulation of several pro-inflammatory chemokines that suppress inflammation, suggesting that shear stress dynamics are capable of directly modulating ECM degradation programs through distinct transduction pathways during the progression of AAA. This evidence concerns the gene SRPX2 and triple-A syndrome.